Fully human IgG1-like bispecific monoclonal antibody targeting EGFR and MET for dual receptor blockade with potential Fc-mediated effector functions.
Fully human IgG1-like bispecific monoclonal antibody that binds EGFR and MET to block ligand binding and receptor activation, suppressing downstream signaling (e.g., MAPK and PI3K/AKT) with potential Fc-mediated effector functions such as ADCC/ADCP against target-expressing tumor cells.
IgG1-like bispecific antibody binds MET on target cells and engages Fcγ receptor–bearing immune cells to elicit ADCC/ADCP (and possibly CDC), killing MET-expressing cells.
T cells from the patient’s previous stem-cell transplant donor engineered to express an anti-CD5 chimeric antigen receptor to target CD5 on malignant T cells and induce CAR T-cell cytotoxic activity with expected on-target depletion of normal CD5+ T cells.
Allogeneic T cells from the patient’s prior stem-cell transplant donor are engineered to express an anti-CD5 chimeric antigen receptor. CAR engagement of CD5 on malignant T cells triggers CD3 zeta and costimulatory signaling, activating the T cells to kill targets via perforin/granzyme-mediated cytotoxicity and cytokine release, with expected on-target depletion of normal CD5+ T cells.
Anti-CD5 CAR T cells bind CD5 on target cells and, upon CAR activation (CD3zeta/co-stimulation), kill them via perforin/granzyme-mediated cytolysis (and Fas/FasL signaling).
B7-H3–targeting antibody-drug conjugate that binds B7-H3 on tumor cells to deliver a cytotoxic payload.
Humanized anti–B7-H3 (CD276) IgG1 antibody-drug conjugate that binds B7-H3 on tumor cells, is internalized, and releases a topoisomerase inhibitor payload, inhibiting DNA topoisomerase activity to block DNA replication, leading to cell-cycle arrest and apoptosis in B7-H3–expressing tumor cells.
An anti–B7-H3 antibody-drug conjugate binds B7-H3 on tumor cells, is internalized, and releases a topoisomerase inhibitor payload that blocks DNA replication, leading to cell-cycle arrest and apoptosis of B7-H3–expressing cells.
Autologous tumor-infiltrating lymphocyte (TIL) product; patient-derived TILs are isolated from the tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens/tumor-associated antigens via the T-cell receptor, mediating CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ support.
Autologous tumor-infiltrating lymphocytes isolated from the patient’s tumor are expanded ex vivo and reinfused. These T cells recognize tumor neoantigens/tumor-associated antigens via their native T-cell receptors (MHC-restricted) and mediate anti-tumor activity through CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ T-cell support, enhancing local immune attack and remodeling the tumor microenvironment.
Autologous TILs recognize patient-specific neoantigen peptides on HLA class I via native TCRs and directly kill target cells through cytotoxic T-cell effector functions (perforin/granzyme-induced apoptosis and Fas–FasL), with IFN-γ support.
Autologous tumor-infiltrating lymphocyte (TIL) product; patient-derived TILs are isolated from the tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens/tumor-associated antigens via the T-cell receptor, mediating CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ support.
Autologous tumor-infiltrating lymphocytes isolated from the patient’s tumor are expanded ex vivo and reinfused. These T cells recognize tumor neoantigens/tumor-associated antigens via their native T-cell receptors (MHC-restricted) and mediate anti-tumor activity through CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ T-cell support, enhancing local immune attack and remodeling the tumor microenvironment.
Autologous TILs recognize tumor-associated peptides presented on MHC I via their native TCRs and directly induce apoptosis of target cells through CD8+ cytotoxicity (perforin/granzyme and Fas–FasL), with IFN-γ support.